Paricalcitol counteracts the increased contrast induced nephropathy caused by renin-angiotensin-aldosterone system blockade therapy in a rat model.

OBJECTIVE: The effect of vitamin D and renin-angiotensin-aldosterone system blockade medications in pathophysiology of contrast induced nephropathy (CIN) is controversial. The effects of paricalcitol (active vitamin D analogue) and losartan treatments in an experimental model of CIN were investigated in this study. MATERIALS AND METHODS: Thirty-six male Wistar albino rats were examined in five treatment groups. Placebo group (Group A; n = 4) received no active medication; control group (Group B; n = 8) received only contrast media (CM); Group C (n = 8) received paricalcitol; Group D (n = 8) received losartan and Group E (n = 8) received paricalcitol plus losartan. CIN was induced by NG-nitro-L-arginine methyl ester and indomethacin before iohexol injection. Renal histopathological findings were categorized and renal immunohistochemical examinations by caspase-3 rabbit primary antibody were performed. RESULTS: Creatinine and cystatin C levels significantly increased in the treatment groups, compared to Group A. However, creatinine levels were not significantly increased in Groups C, D and E compared to Group B. Compared to Group B, a significant increase of cystatin C levels was observed in Group D (p < 0.01). In Group E, when paricalcitol treatment was added to losartan treatment, cystatin C levels were similar to Group B (p = 1.00). In histopathological and immunohistochemical examination frequency of Grade 2/3 tubular necrosis and renal caspase 3 activity scores were significantly higher in the losartan treatment group compared to the other treatment groups. The histopathological effects related to losartan treatment were found to be reversed when paricalcitol treatment was combined. CONCLUSIONS: Our findings suggest that paricalcitol treatment counteracts increased contrast induced nephropathy caused by losartan. These findings warrant further clinical studies to investigate the benefit of paricalcitol in CIN prophylaxis.

A decreased serum omentin-1 level may be an independent risk factor for peripheral arterial disease.

AIM: Recent evidence suggests that omentin-1, a visceral adipose-derived cytokine, may play a role in atherosclerosis The aim of this study was to evaluate whether serum omentin-1 levels are associated with peripheral artery disease (PAD) and its severity. METHODS: The present study was cross-sectional and observational. We enrolled 123 patients with PAD and 50 age-matched subjects without PAD. The cardiovascular risk factors, ankle-brachial index (ABI), and serum omentin-1 levels were assessed in all participants RESULTS: Patients with PAD had significantly lower omentin-1 levels than those without PAD (206. ±48.4 vs. 345. ±80 ng/mL, respectively; 0.001). A correlation analysis revealed positive correlations between the omentin-1 level and the ABI ( 0.52, P=0.008). After adjusting for cardiovascular risk factors, a decreased omentin-1 level was found to be an independent predictor of both PAD and its severity as measured by ABI in multivariate logistic regression analysis. CONCLUSION: The current study suggests a strong association between decreased serum omentin-1 levels and PAD and its severity. Thus, omentin-1 may be a novel biomarker for PAD.

[The effects of application of rectal naproxen on postoperative analgesia, sedation and morphine use in heart surgery operations]. / Kalp cerrahisinde rektal naproksenin postoperatif analjezi, sedasyon ve morfin kullanimi üzerine etkileri.

In this study, effects and side effects of application of rectal naproxen, combined with patient controlled intravenous morphine analgesia, were investigated in the elective coronary bypass operations for postoperative pain control, sedation and opioid use. Following the ethical committee approval and individual patient self consent, 40 patients, who underwent coronary artery bypass surgery were included in the study. A double blind study was performed by administering rectal naproxen to group N (n = 20) and placebo to group P (n = 20), at the end of the operation. Doses were repeated at the 12th hour postoperatively. Patient controlled intravenous morphine analgesia was performed to all patients for postoperative 24 hours. Postoperative pain and sedation levels were assessed, the side effects were noted. There was no difference between two groups with respect to their demographic features duration of surgery, extubation time and side effects (p > 0.05). With respect to group P, decrease in opioid use, better sedation and decrease in pain scores during both resting and coughing was seen in group N (p < 0.05). In conclusion, analgesia applied by addition of rectal naproxen to opioids achieved better pain management in selected patients after cardiac surgery.